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105 Cards in this Set

  • Front
  • Back
HIPAA
Health Insurance Portability & Accountability Act of 1996
HIPAA goals
1) protects PT's info
2) provides for appropriate uses
3 acceptable uses for PHI
1) treatment
2) payment
3) operations
Minimum Necessary Rule
least info possible to complete task
golden rule
everything seen and heard should be left at the scene
golden rule does not apply to
-PT treatment
-billing
-quality assurance
-critical incident situation debriefing
Dispatch and response acceptable uses
-sharing info with other units
-talking to family members
-info to and from bystanders
-ok to transmit PHI to hospital
-ok to transfer PCR
After the call acceptable uses
-discussions with crew
-QA/CISD
Law Enforcement Disclosures
-we are PT advocates
-drinking - no
-health stuff ok
Notice of Privacy Practices
get signature for non-emergent patients
-emergent not req'd
Mass Casualty Incidents
ok to disclose PHI
PT acess
Direct PT to admin

-PT may request ammendment of info, we are not obligated to change
Safeguarding PT info (3 catagories)
1) Written - locked cabinet role based

2) Verbal - use most secure method to tansmit, be aware of voice volume

3) Electronic - password protection fax with cover sheet
victim of a crime
tell law enforcement
Breakdown of water types in the body
60% water weight

Plasma - 4%
Interstitial Fluid - 16%
Intracellular Fluid - 40%
What happens as the body begins to sweat?
liquid leaves the skin via the ICF/ECF, fluid leaves the blood stream to replace
Fluids IV (3 types)
Hypotonic - low concentrate levels - pure water

Hypertonic - high concentrate levels - D50 (dextrose)

Isotonic - same level of stuff - 0.9% NaCl
How does R sided CHF affect blood pressure?
increased venous pressure (up from 2-10)

causes edema
normal arterial and venule pressures
arteriole - 120

venule - 2-10
Edema pooling locations
ambulatory - legs and feet

non-ambulatory - butt
pH
Potential for Hydrogen


ACID 1 ------------------------14 BASE

acids donate hydrogen ions, bases receive
Normal pH operating range
7.35-7.45
3 Balancing Methods
1) Renal = (Days) Effective but slow
-recapture Bicarb, secrete H+

2) Respiratory = (minutes) middle effectiveness

3) Carbonic Acid = (instant) not very effective
-ICF
Carbonic Acid
H2CO3

-temporary portal to either side of equation
Carbonic Acid Full Equation
H2O + CO2 <-> H2CO3 <-> H + HCO3
4 IMBA's
OD with bicarb = metabolic alkalosis

Pooping = metabolic acidosis

Not Breathing = respiratory acidosis

Hyperventilation = respiratory alkalosis
Ex. Cyanosis with clear lungs ?
pulmonary embolism, no blood gets to the lungs to profuse
Normal Operating Range for PO2 and PCO2 in body
PO2 = 80-100 Normal

PCO2 = 35-40 Normal
Is P02 affected in metabolic acidosis or alkalosis?
No
PH 7.2
PO2 40
PCO2 80
RR 4
Respiratory Acidosis,

RR is extremely slow, PO2 is bad
PH 7.2
PO2 40
PCO2 80
RR 36
Respiratory Acidosis

Ineffective Respiration's due to CHF
PH 7.7
PO2 100
PCO2 80
RR 8
Metabolic Alkalosis

No hyperventilation, RR is trying to compensate
PH 7.8
PO2 90
CO2 20
RR 8
Metabolic Alkalosis
PH 7.33
PO2 80
PCO2 60
RR 30
Metabolic Acidosis

O2 is fine, RR is trying to compensate
PH 7.8
PO2 100
PCO2 30
RR 36
Respiratory Alkalosis

PO2 is fine RR is way too high
PH 7.8
PO2 100
PCO2 20
RR 8
Metabolic Alkalosis

PO2 is fine, RR is low
PH 7.2
PO2 40
PCO2 80
RR 8
Respiratory Acidosis

PO2 is bad, RR is slow.
Types of Shock (5)
1) Hypovolemic - volume is too low
-dehydration slow
-hemorrhagic - fast

2) Cardiogenic - Heart damage due to tissue death ) 40% heart DMG is fatal

3) Nuerogenic Shock - loss of sympathetic motor tone
-arterioles begin to dilate

4) Anaphylactic shock - severe allergic reaction
-fluid moves to tissue, BP bottoms out, airways constrict

5) Septic Shock - systemic bacterial infection
-fluid is fine, cells can't unload toxins properly
Baroreceptors Location and function
located in arch of aorta, R atria, carotid arteries

react to pressure change, satisfied (BP ok), unsatisfied (BP low)
-signal to heart to increase rate and strength, increase vasoconstriction
peripheral vascular reistance
affects the pressure of the blood by constricting
catecholomines
hormones that stimulate A1, A2, B1, B2

Epinephrine
A/B receptors location
Alpha 1 = arterioless
Beta 1 = heart
Beta 2 = lungs (dilate bronchioles)
Vascular properties
arteries - very elastic

arterioles - muscles change in size, tight = high BP

Capillaries - no change in size
4 Basic Types of tissue
1) Epithelial tissue

2) Connective tissue

3) Muscle tissue

4) Nervous tissue
Who has more water content babies or old people? male or female? fat or skinny?
Males, Babies, and Skinny people have a higher water content
Mediated Transport Mechanisms
Required to move large water soluble molecules or electrically charged molecules across cell membranes,
Active Transport vs Facilitated Diffusion
Active transport moves molecules against a concentration gradient, lower to higher

Facilitated Diffusion is passive and molecules go from areas of high to low concentration. with the gradient. no energy required
arterioles & metarterioles components
arterioles > Metarterioles > Capillaries

either true capillaries or thoroughfare channels which bypass the capillaries and connect arterioles and venules

Precapillary Sphincters control blood flow through the capillaries
AV shunts
non-nutritional/shunt flow, help regulate body temp, found in sole of the foot, palm of the hand, phalanges and nail bed
Regulation of blood vessels
both vasoconstrictor and vasodilator, sympathetic system is the most important.
normal circulation characteristics
arterioles are open, AV shunts closed, 20% capillaries open at a given time
Diffusion across the capillary wall
nutrients diffuse across the capillary wall into the interstitial fluid to enter the cells.

Metabolic end products diffuse across cell membrane into the extracellular fluid
Starling's Hypothesis
Net Filtration = Forces Favoring Filtration - Forces opposing filtration

At arteriole end - filtration
+HIGH Blood pressure
+LOW negative interstitial pressure
-LOW Blood colloid osmotic pressure (low because lots of fluid still in)

Venous End - inward forces
-HIGH Blood Colloid osmotic pressure (low fluids in vessel, so high particle concentration)
+LOW blood pressure
+LOW negative interstitial pressure
membrane permeability
if permiability changes, particles may escape from the lumen into the interstitial space, lowering the blood oncontic pressure. Edema results
4 Factors causing edema
1) Increase in the hydrostatic pressure

2) Decreased Plasma Oncotic Pressure

3) Increased Capillary Permeability

4) Lymphatic obstruction
localized vs generalized edema
localized is limited to an injury site or an organ system (sprained ankle)

generalized is widespread swelling due to chronic conditions including heart disease, kidney, and liver disease
ADH
antidiuretic hormone - helps to regulate water balance

-released with high plasma osmolality or a decrease in circulating blood volume

-puts aquaporins in the DCT of nephrons reclaims most of the water in urine
Normal ratio of carbonic acid to bicarbonate
20 : 1 at pH of 7.4
what determines our respiratory rate?
the pH

hemoglobin binds with carbon dioxide and hydrogen ions. at the lungs the hydrogen ions combine with bicarb forming Carbonic acid which becomes CO2 and H2O, which is exhaled
Renal Buffering Components (3)
1) recovery of bicarb

2) secretion of hydrogen ions into urine

3) excretion of ammonium ions, which carry a hydrogen ion with it
Respiratory Acidosis symptoms
-respiratory depression
-respiratory arrest
-cardiac arrest
-neuromuscular impairment
-medications (sedatives, hypnotics)
-chest wall injury
-pulmonary disorders
4 Main causes of Metabolic Acidosis
1) Lactic Acidosis
-the body switches from aerobic to anaerobic respiration, creating lactic acid which releases hydrogen ions

2) Diabetic Ketoacidosis
-pt fails to take enough insulin, fatty acids are metabolized producing ketone bodies and releasing hydrogen ions

3) Acidosis by renal failure
-kidneys reclaim bicarb and release Hydrogen if working properly

4) Acidosis caused by ingestion of Toxins
Respiratory Alkalosis can be caused by...
hyperventilation
Mixed acid-base disturbances are commonly seen in pt's with what condition?
SHOCK
5 most signifcant adaptive changes in cells
1) atrophy - decrease in size

2) hypertrophy - increase in size

3) hyperplasia - excessive increase in the number of cells (in a row)

4) metaplasia - a change from one cell type to another that is better able to tolerate adverse conditions (not normal for that cell type)

5) dysplasia - abnormal changes in mature cells
Hypoxic injury
cell damage

lack of oxygen due to athersclerosis or thrombois leads to infarction or cell death
Chemical Injury
cell damage

toxins or chems may affect cell membrane permiability, or disrupt cellular metabolism
Infectious Injury
cell damage

bacteria create exotoxins, they carry the genetic material to make the toxin
-also activate the inflammatory process

virusus - genetic material encapsulated, require a host to replicate
Immunological & inflammatory injury
cell damage

cells are damaged by the cells causing inflammatory responses, as well as complement

If the Na/K pump breaks, the cell may swell and rupture
Genetic Factors
cell damage

inherited abnormal cell characteristics
Nutritional Imbalances
cell damage

rickets, scurvey, obesity etc
physical agents
cell damage

-temperature extremes, atmospheric pressure, radiation, illumination, mechanical stress
Cellular manifestations of injury (3)

what happens when cells are injured?
1) cellular swelling
resulting from membrane changes, K out Na in. Water follows Na, increased swelling

2) Fatty Change
-enzyme systems that metabolize fat are impaired and overwhelmed. lipids accumulate inside the cell

3) system manifestations
-fever, malaise, loss of well being, change in appetite, altered heart rate and rise in WBC
shock
decreased cardiac output, hypoprofusion
cardiac output
depends on several factors, including strength of contraction, rate of contraction and he amount of blood returning through the veins.


SV X HR
chemoreceptor reflexes
compensatory mechanism

found in the carotid and aortic bodies, activated by PO2 or pH decrease, vasomotor center of the medulla stimulated, rate and depth of ventilation increased

can also stimulate vasomotor to enhance PVR
central nervous system ischemic response
compensatory mechanism

blood flow to the vasomotor center of the medulla. nuerons in the vasomotor center become excited, raising the arterial blood pressure

does not activate until the blood pressure falls below 50mmHg

10 minute duration
Hormonal mechanisms that increase BP
compensatory

1) renin-angiotensin-aldosterone & vasopressin
(renin released by kidneys, becomes angiotensin 2 in lungs = vasoconstriction)

2) aredenal medulla secretes epi and noreppie

3) vasopressin (ADH)
Splenic discharge of blood
some of the blood that circulates through the spleen is stored in an area called the venous sinususes. (300ml) expelled during hypotension
reabsorption of tissue fluids
lowered BP means less hydrostatic pressure, less fluid moving into the capillaries
MODS
multiple organ dysfunction syndrome

triggered by the body's inflammatory response

consists of 3 systems
-complement (further damages epithelial membrane)
-coagulation
-kallikrein (vasodilation)

Hyperdynamic circulation > increase demands on the heart > depletion of O2 and fuel > decreased O2 to cells/hypermetabolism/myocardial depression > multiple organ failure > tissue hypoxia
Impairment of cellular metabolism
-anerobic production of ATP inefficient, releases lactic acid and hydrogen ions

-ions begin to accumulate, causing vasodilation

-post capillary sphincters resistant, so capillaries more permeable, fluid enters ECF

-inefficent ATP production hinders Na/K pump, causing decreased membrane potential and eventually cell damage
3 lines of body defense
1) external barriers, skin and mucous membranes

2) inflamatory response

3) immune response
inflammatory response 3 stages
1) cellular response to injury
-damage to cell causes membrane permiability, organelle permiabiity, hydrolytic enzymes release and the cell undergoes apoptosis

2) Vascular response to injury
-increased blood flow to injured area causes edema luekocytes begin to gather along the vascular endothelium as a result of chemical attractants.

3) phagocytosis
-luekocytes engulf, digest, and destroy pathogens, eventually lysis occurs and pus is created
MAST cells
cytoplasm is filled with granules containing vasoactive amines and chemotactic factors

stimulated by trauma, or physical injury, or chemical agents (bee sting)

cause inflammation
local vs system responses to acute inflammation
local
-vascular changes (vasodilation)
-formation of pus

systemic
-fever
-leukocytosis
-increase in circulating plasma proteins
response to chronic inflammation
inflammation that lasts 2 weeks or longer

-connective tissue fibers and new blood vessels
-large area = scar tissue forms
Acquired immunity
exposure to a specific antigenic agent or pathogen
-exposure can be in the form of a vaccination
Humoral Immunity VS Cell mediated Immunity
Both considered acquired immunity

humoral immunity
-production of antibodies that combine and kill the invader

cell mediated immunity
-formation of a group of lymphocytes that attack and destroy foreign material
antigen vs immunogen and components of
antigen is a substance that reacts with preformed components of the immune system

immunogen is a specific type of antigen that can bring about or induce the formation of antibodies. they must be
-sufficiently foreign to the host
-sufficiently large
-sufficiently complex
-present in sufficient amounts
creation of B and T cells and differences between
phagocytes digest foreign material and antigenic material appears on their surface.

-some mature into B Plasma cells that produce antibodies
-some mature into sensitized T lymphocytes that directly hunt and kill the antigen
Universal Donor vs. Recipient and Rh factor
Universal donor is O

Universal Recipient is AB

A has anti B antibodies
B has anti A antibodies
O has both antibodies
AB has none

Rh factor is another protein 85% of people have it.
allergy, autoimmunity and isoimmunity
allergy - refers to an exaggerated immune response by environmental allergens (most common, least life threatening)

autoimmunity - immune response against the host's own cells

isoimmunity - immune response directed against beneficial foreign tissues (blood transfusion)
IgE reactions
accounts for less then 1% of the AB in normal serum

-responsible for immediate (type I) hypersensitivity reactions.
-bound to mast cell or basophils, cause these cells to release chemical mediators when antigens bind
IgG
70-73% of the antibodies in serum

most abundant in blood, but found in lymph, cerebrospinal fluid, synovial, pertioneal fluid, breast milk

-secondary immune response
-crosses placenta
IgM
5-10%
-trigger increased production of IgG in acute infections and complement fixation required for an effective AB response
IgA
15%
-blood, tears, saliva, RT, stomach, organs

-combines with a protein in mucosa that defends body surfaces agains invading microorganisms
IgD
less then 1%

unknown function
Acquired Deficiencies 5 groups
Much more common then congenital forms

1) nutritional deficiencies

2) Iatrogenic deficiencies (caused by some form of medical treatment)

3) deficiencies caused by trauma (bacterial infections, burns)

4) deficiencies caused by stress (depressed immune function)

5) Acquired Immunodeficiency Syndrome (AIDS)
psychoneuroimmunology
study of the three way interaction of the emotional state, the central nervous system, and the body's defense against external infection and abnormal cell division
stress response
activates the sympathetic nervous system

catecholomines (eppie/noreppie, and dopamine) released into the blood stream

hypothalamus stimulates the pituitary gland to release ADH, prolactin, growth hormone, and adrenocorticotropic hormone (ACTH)

ACTH stimulates the cortex of the adrenal gland to release cortisol
cortisol effects what?
stimulation of gluconeogensis, by reducing glucose utilization

slows down immune cell activity, helps prevent damage
factors that cause disease
genetics, environment, age and gender
analyzing the risk of disease
incidence/prevalence/mortality rate

causal risk factors/noncausal risk factors
familial disease tendency
due to genetic factors or shared environmental factors